ArticlePloS one2017
Effects of prenatal low protein and postnatal high fat diets on visceral adipose tissue macrophage phenotypes and IL-6 expression in Sprague Dawley rat offspring.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Key questions and gaps in understanding adipose tissue macrophages and early-life metabolic programming.American journal of physiology. Endocrinology and metabolism · 2024Review
- Visceral fat and cardiometabolic future in children and adolescents: a critical update.Pediatric research · 2023Review
- Animal Foetal Models of Obesity and Diabetes - From Laboratory to Clinical Settings.Frontiers in endocrinology · 2022Review
- Cardiometabolic Effects of Postnatal High-Fat Diet Consumption in Offspring Exposed to Maternal Protein RestrictionFrontiers in physiology · 2022Review
- Developmental programming of offspring adipose tissue biology and obesity risk.International journal of obesity (2005) · 2021Review
- Mediterranean Diet for the Prevention of Gestational Diabetes in the Covid-19 Era: Implications of Il-6 In Diabesity.International journal of molecular sciences · 2021Review
- Pregestational diet transition to normal-fat diet avoids the deterioration of pancreatic β-cell function in male offspring induced by maternal high-fat diet.The Journal of nutritional biochemistry · 2020Article
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- Opposing Actions of Developmental Trichloroethylene and High-Fat Diet Coexposure on Markers of Lipogenesis and Inflammation in Autoimmune-Prone Mice.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Adipose tissue macrophages (ATM) are implicated in adipose tissue inflammation and obesity-related insulin resistance. Maternal low protein models result in fetal programming of obesity. The study aims to answer whether maternal undernutrition by protein restriction affects the ATM M1 or M2 phenotype under postnatal high fat diet in F1 offspring. Using a rat model of prenatal low protein (LP, 8% protein) diet followed by a postnatal high fat energy diet (HE, 45% fat) or low fat normal energy diet (NE, 10% fat) for 12 weeks, we investigated the effects of these diets on adiposity, programming of the offspring ATM phenotype, and the associated inflammatory response in adipose tissue. Fat mass in newborn and 12-week old LP fed offspring was lower than that of normal protein (20%; NP) fed offspring; however, the adipose tissue growth rate was higher compared to the NP fed offspring. While LP did not affect the number of CD68+ or CD206+ cells in adipose tissue of NE offspring, it attenuated the number of these cells in offspring fed HE. In offspring fed HE, LP offspring had a lower percentage of CD11c+CD206+ ATMs, whose abundancy was correlated with the size of the adipocytes. Noteworthy, similar to HE treatment, LP increased gene expression of IL-6 within ATMs. Two-way ANOVA showed an interaction of prenatal LP and postnatal HE on IL-6 and IL-1β transcription. Overall, both LP and HE diets impact ATM phenotype by affecting the ratio of CD11c+CD206+ ATMs and the expression of IL-6.
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